Increasing body fat content in recent-onset type 2 diabetes mellitus (T2DM) appears to lead to the accumulation of hepatocellular lipid (HCL), a recent study has found.
The study included 30 patients with type 1 diabetes mellitus (T1DM) and 37 with T2DM. To measure HCL, inorganic phosphate (Pi) and γ-adenosine triphosphate (ATP), the researchers conducted 1H/31P magnetic resonance spectroscopy at diagnosis and 5 years later. Hyperinsulinaemic-euglycaemic clamps were used to assess insulin sensitivity.
In T2DM patients, 5-year changes in HCL were collected with body mass index (BMI; r, 0.44) and serum triglycerides (r, 0.50), as well as with whole-body (r, 0.51) and subcutaneous (r, 0.49) adipose tissue. Adipose tissue insulin resistance was likewise associated with HCL changes (r, 0.44; p<0.05 for all).
At the same time, hepatic γATP was negatively correlated with BMI and whole-body fat (r, –0.71; p<0.05 for both), and positively associated with baseline fasting hepatic insulin resistance (r, 0.65; p<0.05). Hepatic Pi at 5 years was also linked to whole-body fat content at baseline (r, 0.63; p<0.05).
Regression analysis found that the increase in HCL over 5 years was significantly and positively correlated with visceral adipose tissue volume (β, 0.001; p<0.05) in both T1DM and T2DM patients combined. The same was true for glycated haemoglobin and serum triglycerides.
“Previous studies suggested that the impaired function of mitochondria, the power plants of cells, can promote fatty liver and T2DM,” the researchers said. “This study now shows that during the first 5 years of T2DM, the increase in body fat content rapidly leads to a doubling of liver fat content, whereas the energy metabolism of the patients’ livers progressively declines.”
“These data suggest that fat tissue mass and liver mitochondria have an important role in the development of fatty liver disease in humans with diabetes,” they added.